期刊
EPIGENETICS
卷 6, 期 2, 页码 128-133出版社
LANDES BIOSCIENCE
DOI: 10.4161/epi.6.2.13625
关键词
DNA methylation; meCpG; DNA methyltransferase-inhibition; DNMT1(-/-); DNMT3b(-/-); aza-deoxycytidine; gene silencing; ribosome biogenesis; cancer therapy
资金
- Canadian Institutes of Health Research (CIHR) [MOP12205]
- FRSQ (Quebec)
Mutations in the pattern of CpG methylation imprinting of the human genome have been correlated with a number of diseases including cancer. In particular, aberrant imprinting of tumor suppressor genes by gain of CpG methylation has been observed in many cancers and thus represents an important alternative pathway to gene mutation and tumor progression. Inhibitors of DNA methylation display therapeutic effects in the treatment of certain cancers and it has been assumed that these effects are due to the reversal of mutant gene imprinting. However, significant reactivation of imprinted tumor suppressor genes is rarely observed in vivo following treatment with DNA methylation inhibitors. A recent study revealed an unexpected requirement for CpG methylation in the synthesis and assembly of the ribosome, an essential function for cell growth and proliferation. As such, the data provide an unforeseen explanation of the action of DNA methylation inhibitors in restricting cancer cell growth.
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